Left ventricular (LV) remodeling caused by a myocardial infarction (MI) is responsible for almost 70% of the 5 million cases of heart failure that have occurred in the United States in recent years. Early infarct expansion or stretching has been associated with poor long-term prognosis and has been identified as the mechanical phenomenon that initiates and sustains the process of adverse post-MI LV remodeling that leads to heart failure.
Infarct expansion causes abnormal stress distribution in myocardial regions outside the infarction, especially in the adjacent borderzone (BZ) region, which stress distribution puts this region at a mechanical disadvantage. With time increased regional stress is the impetus for several maladaptive biologic processes, such as myocyte apoptosis and matrix metalloproteinase activation that inherently alter the contractile properties of normally perfused myocardium. Once initiated, these maladaptive processes lead to a heart failure phenotype difficult to reverse by medical or surgical means.